Protozoal Infection

8/2/2019 Protozoal Infection

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Entamoeba histolytica Giardia Lamblia Balantidium Coli Isospora Belli Cryptosporidia

Phlum,

Subphylu

m

SM, Sarcodina SM, Mastigophora Ciliophora Apicomplexa Apicomplexa

geo dist cosmopolitan but tropical & subtropical

countries >

cosmopolitan but tropical &

subtropical countries >

cosmopolitan

most common in tropical

zones esp philippines

cosmopolitan but

tropical & subtropical

>

cosmopolitan

habitat trophozoites and cysts 1rily inhabitthe lumen of LI

occasionally trophozoites invademucosal crypts where the lyse

tissues, feed on RBC, form ulcers

crypts of duodenum + upperjejunumoccasionally in bile ducts and

gall bladder

caecum and colon of

humans, pigs, guinea pigs,rats and other mammals

epithelial cells of

distal duodenum andprox jejunum

originally para of calves

but can infect man,kittens, puppies, rodents

morpho fresh unstained

faecal smear

H&E

o bilaterally symmetricalo pear-shaped broad antly and

tapering postly

o 9-21 x 5-15 o Dorsal surface convexo Ventral surface ant ovoidal

concavity (sucking disc)

serves as attachment tomucosa

o 2 vesicular nuclei in area ofsucking disc

o 4 pairs of flagella + 2 sausageshaped median bodies post

to sucking disc

o Multiply repeated by binaryfission

30-150 x 25-120

Oblong/ spheroid Ant end - peristome,

either wide open OR

slit like

Post end - cytopyge Whole body covered w

fine cilia arranged inrows

1 macronucleus- v slightly curved

kidney or bean shaped

- lies obliquely near

middle of body

- about 2/5 of length of

body

1 micronucleus- much smaller

- often hidden

2 contractile vacuoles ;1 near middle of body,

1 near post end

Food vacuoles containcell fragments, starch

granules, faecal debris,

RBC

TROPHOZ

OITES

pseudopodium w

clear ectoplasm

+

nucleus not visible

+

ingested RBC -> v

pale greenishrefractile bodies

20-60

ectoplasm clearly

differentiated from

endoplasm

+

spherical nucleus w

small central

karyosome+

fine granular

chromatin granules

lining the nuclear

membrane

+

ingested RBC ->

bluish black dics in

endoplasm


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CYSTS spherical / oval

bodies w a hyaline

refractile cyst

+

nuclei may not be

visible OR

1-4 hyaline bodies

+

chromatid bodies

made up of RNA ->rod shaped clear

areas in cytoplasm

10-20

nuclear structure is

apparent and

similar to trophic

form

+

mature cyst

contains 4 visible

nuclei

+

chromatid bodies -> rod shaped +

rounded edges &

stain blue black

o oval in shapeo 8 x 14 o 4 nuclei usually at one poleo Parabasal bodieso Remnants of flagellao Axonemeso Encystations occur when

liquid faeces become

dehrydrated in transit down

the colon

Spheroidal / ovoidal w40-60 diameter and

thick cyst wall

Macro and micronuclei can also be seen

(mature sporulated

oocyst)

20-33 x 10-19

Contain 2mature

sporocyst with

4 sporozoites

each

(mature oocyst + 4 naked

sporozoites)

4-6 in diameter

reproducti

on

binary fission longitudinal binary fission transverse fission asexual schizogenic

cycle +

sexual reproduction

asexual schizogenic cycle

+

sexual reproduction

def. host humans

infect.

stage

mature 4 nucleated cyst

*if trophozoites are swallowed, they are

destroyed by gastric acidity

cysts cysts mature sporulated

oocyst

mature oocyst + 4 naked

sporozoites

diag. stage

mode of

infection

contamination of food and drink thru :

1. Polluted water supply2. Imperfectly washed raw vege3. Contaminated hands esp in food

handlers who are cyst passers

4. Food contaminated w vomits orexcreta of flies since the cysts pass

unharmed thru intestine of these

insects

5. Usage of human excreta as fertilizers

ingestion of food or water

1. Contaminated of food and drink2. Direct infection from man to man3. Autoinfection4. Mechanical transmission by house

flies

endemic areas : infection occurs ano-

orally directly from one to another

epidemic areas : infection thru

polluted water supplies

more common in children

ingestion of cyst

usually in

contaminated water or

food

basically it is a parasite

of pigs, and is esp

common in ppl who

are in close cntct w

pigs

ingestion of water or

food contaminated

with mature

sporulated oocysts

ingestion of mature

oocysts thru:

1. Contamination offood and drink by

oocysts

2. Close cntct withinfected calves

3. Auto-infection4. Direct person to

person

5. Inhalation


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patho-

genesis

pathological changes depend on : Virulence of infective strain Host resistance Host nutritional status Bacterial infection

most affected areas (dt sluggishmovement of faecal material :

Caecum Rt & Lt colic flexures Sigmoid colon

pathogenic trophozoites secretelytic enzyme

small areas of necrosis in epithelium

giving a way to penetrate

(penetration)

erode into deeper tissues breaking thru

musc. Mucosa

(reach submucosa)

where the spread fan-like, multiply

extensively causing lytic necrosis (when necrotic content

is

discharged)

typical flask shaped ulcers produced,

mucosa in between is healthy

further progress invasion may occur thru

penetration of musculosa and reaching

serous coat peritonitis

amoebiasis of caecum appendix

amoebic appendicitis

chronic infection + superadded bactinfection granulomatous nodular

mass (amoeboma)

erosion of BV in the wall of ulcers hemorrhage amoeba carried by

BV as emboli to reach liver and

others

under ordinary

conditions,

trophozoites feed on

food debris in caecum

but sometimes,

organism can produce

proteolytic enzyme

digest away

epithelium ulcer

ulcer mayb rounded

irregular OR flask

shaped

+

narrow neck

undermining sac-like

cavity in submucosa

colonic ulceration

lymphocytic infiltration

w fewpolymorphnuclear cells

+ hemorrhage

2ry bacterial invasion

may follow

distortion of

intestinal villi +

cellular infiltration of

plasma cells,

lymphocytes,

eosinophils


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clinical pic ASYMPTOMATIC (major of cases, 80-90%)

patient is a carrier of cysts

this person is in danger to himself

and to others

SYMPTOMATICINTESTINAL LESION

1. Acute dysentery variable incub. period : as short

as 4 days, as long as a year

gradual onset except infulminating cases where it is

sudden

gripping abd pain + dysentery(diarrhea + tenesmus + blood +

mucus in stool)

localized abd pain over caecumand pelvic colon

no of motions are 4-8 per day

toxemic manifestations are rare

2. Non Dysenteric Colitis Vague abd discomfort +

distention of caecum and colon

+ gas

Diarrhea alternating wconstipation may be present

3. Amoeboma / AmoebicGranuloma

Results from repeated amoebicinfection + superadded bact

infectionmass in abdmight

be misdiagnosed as carcinoma

Surgical removal w/out medicaltreatment is fatal

good % are asymptomatic

in symptomatic cases, IP last from 1-3

weeks and present itself in diff forms:

Diarrhea

gradual / acutestool are offensive, pale yellow and

frothy similar to lentil soup

Dyspepsia

epigastric pain, marked nausea,

flatulence

Malabsorption

severe infection resembles tropical

sprue :

weight loss lassitude fatty stools

fatty stool dt :1. attachment of sucking disc tomucous membrane

blockage of mucosal cells

absorption of FA

2. inflammation of epithelial cells

absorption capacity

both of these conditions lead toaccumulation of unabsorbed FA

fatty yellow frothy stools

there is also malasorption of D-

xylose and vit B12

may be asymptomatic

but major of cases

present with

1. dysentery2. abd colic3. tenesmus

resembling

amoebic

dysentery4. intestinal

perforation

(fulminant case)

5. invasion ofextraintestinal

such as liver

(rare)

1. diarrhea forseveral months

to years

+

weight loss

+

abd colic

+

fever

2. bowel motions,6-10x daily

3. soft to watery,foamy + offensive

smell =

malabsorption

4. profuse diarrhea+ weakness +

anorexia + weight

loss inimmunosuppress

ed patients

(AIDS)

1. low grade fever2. abd cramps3. diarrhea, self

limited in person

w normal

immune

response BUT

fatal in immuno-

compromized

patients4. respi infection


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EXTRAINTESTINAL

1. Amoebic Hepatitis Results from emboli of trophozoites

from LI reaching liver via portal

blood no of small necrotic foci, if

not treated, coalesce to form abcess

Acute onset : may occur duringattack of dysentery / in ppl who gaveno history of amoebiasis at all

Sudden rise in temp + enlargedtender liver

2. Amoebic Liver (Liver Abcess) dt untreated amoebic hepatitis toxemic manifestations are more

severe, pain becomes stabbing

referred to rt shoulder and increase

by coughing and inspiration and

relieved by lying on rt side patient has a characteristic muddycomplexion denoting toxaemia

liver is enlarged and tender +marked intercostals edema over site

of liver

abcess may rupture into pleuralcavity, lung, pericardium, stomach,

rt colonic flexure, perinephric area,

gall bladder or skin

3. Pulmonary Amoebiasis Thru invasion of hepatic abcess thru

diaphragm / rarely blood born 1ry

infection from intestinal ulcers

Manifested by dyspnea + lowerchest pain + cough


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4. Cutaneous lesions On skin covering the liver area after

rupture or aspiration of an amoebic

liver abcess OR perineal region in

debilitated infected patients

Manifested by tender swollenulcerated area

5.

Cerebral lesions

Result of blood extension from pre-existing lesion in liver / lung OR

direct hematogenous spread from

colon

May stimulate brain tumour which isusually fatal

COMPLICATIONS

1. Intestinal : hemorrhage,appendicitis, amoeboma

2.

Extraintestinal : amoebichepatitis, amoebic liver, lung

involvement, amoebiasis cutis,

may stimulate brain tumour


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Lab

Diagnosis

DIRECT METHOD DIRECT METHOD stool

examination

to discover

trophozoite w

or w/out

cystic stage

1.stoolexamination

by simple saline

/ iodine smear

conc

techniques

such as zn

floatation maybused if infection

is scanty

organisms are

acid-fast,

oocysts appear

bright pink

when stained w

modified ZN

stain

2. Blood piceosinophilia

1. stool examinationusing formol ether

OR Sheathers

sugar flotation

oocysts are better

visualized when

stained by

modified ZN acidfast stain bright

pink

2. entero test3. intestinal biopsy4. sputum

examination

INTESTINAL

1. Stool examinationDysenteric stool (trophozoite

is visible)

either thru fresh saline smear

OR fixed stool specimen

*refer to morpho

Well formed stool (cyst isvisible)either thru fresh saline/iodine

smear OR fixed stool sample

2. Sigmoidoscopyfor visualization of amoebic

lesion and confirmation of

diagnosis by taking scraped

material from an ulcer

HEPATIC

1. History and clinicalpic of patient

2. X-ray shows upwarddisplacement of

diaphragm + reduced

movement +

sometimes a fluidcan be seen

3. CT scan4. Aspiration ; only if

theres a large abcess

so used as

treatment,

o aspirated material isviscid, choc brown,

thick (anchovy

sauce)

o trophozoites neverfound in pus, theyare only present if

aspirate is taken

from edge of the

abcess

5. Trophozoites can befound in sputum if

liver abcess rupture

into the lung

1. Stool examinationDiarrhoeic stool, trophozoite

is visible in saline smears

Well formed stool, cysts arevisible easily by staining w

Lugols iodine solution

repeated stool examinationshud be done coz organismstend to pass in stools

intermittently

3 samples shud be examined

routinely on alternate days

in scantyinfections,concentration by Zn sulphate

floatation technique is of

value

2. Duodenal aspirationwhen clinical pic is

suggestive of giardial

infection and repeated

stool examination give -

ve results esp that

excretion of parasite is

erratic and not regular

3. Entero test capsule(string test)

INDIRECT METHOD INDIRECT METHOD

indirect haemagglutination test (IHAT), ELISA, and gel

diffusion tests are +ve in invasive amoebiasis : acute

dysentery and amoebic abcess

detection of FL copro Ag in

stools by ELISA technique is

helpful and resorted when

repeatedve results of stool

examination and CP is

suggestive


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treatment choice of drug depends on type of clinical presentation& site of drug action

luminal amoebicides - drugs act 1rily on organisms incolonic lumen mainly cyst passers

tissue/systemic amoebicides - acting on invasive stages(tissue forms)

all patients w invasive disease require treatment 1stly wsystemically acting compound, subsequently w luminal

amoebicide to eliminate any organisms in colon

1. asymptomatic intestinal infection (cyst passers)o diloxanide furoate (furamide)

2. non dysenteric intestinal colitiso diloxanide furoate +metronidazoleo furazole (combination of diloxanide

furoate and metronidazole)

3. dysenteric intestinal colitiso bed rest + fluid and electrolyte replacement

therapy

o specific treatment : metronidazoleaccompanied by furazole

4. hepatic abcesso hospitalization + bed resto needle aspiration is advisablewhen size of

abcess is large and when severe hepatic

pain and tenderness

o specific treatment : metronidazole

metronidazole (flagyl) tetracycline

dose: 500mg,

4x daily for 10

days

cotrimoxazole

a comnbination

of trimethoprim

(TMP) +

sulphamethoxazo

le (SMX)

each tablet made

up of 160mg TMP+ 800mg SMX

dose : 1 tablet

twice daily for

10days

*in immune-

suppressed

pastients w

persistent

infection

treatment shud

be for life

nitazoxanide

Protozoal Infection

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